ACSL5 Antibodies

Long-chain-fatty-acid--CoA ligase 5 (ACSL5)

Acyl-CoA synthetases (ACSL) activate long-chain fatty acids for both synthesis of cellular lipids, and degradation via beta-oxidation. ACSL5 may activate fatty acids from exogenous sources for the synthesis of triacylglycerol destined for intracellular storage (By similarity).

Utilizes a wide assortment of saturated fatty acids with a preference for C16-C18 unsaturated fatty acids (By similarity). It had been suggested that it may also stimulate fatty acid oxidation (By similarity).

Gene Information

Human
Gene Name:	ACSL5
Uniprot:	Q9ULC5
Entrez:	51703

Family

Belongs to:
ATP-dependent AMP-binding enzyme family

Alternative Names

ACS2; ACS5FACL5 for fatty acid coenzyme A ligase 5; acyl-CoA synthetase long-chain family member 5; EC 6.2.1; EC 6.2.1.3; FACL5fatty acid coenzyme A ligase 5; fatty-acid-Coenzyme A ligase, long-chain 5; LACS 5; Long-chain acyl-CoA synthetase 5; long-chain fatty acid coenzyme A ligase 5; long-chain-fatty-acid--CoA ligase 5

Molecular Weight

Mass (kDA):
75.991 kDA

Genomic Context

Human
Location:	10q25.2
Sequence:	10; NC_000010.11 (112374116..112428380)

Subcellular Localizations

Mitochondrion. Endoplasmic reticulum. Mitochondrion outer membrane; Single-pass type III membrane protein. Endoplasmic reticulum membrane; Single-pass type III membrane protein. Cell membrane.

Diseases

• Malignant Neoplasms
• Neoplasms
• Glioma
• Malignant Paraganglionic Neoplasm
• Adenoma
• Malignant Neoplasm Of Brain
• Celiac Disease
• Adenocarcinoma
• Steatosis
• Colorectal Neoplasms
• Carcinogenesis
• Colorectal Cancer
• Malignant Glioma

• Obesity
• Autoimmunity
• Stomach Neoplasms
• Malignant Neoplasm Of Breast
• Neoplasms, Experimental
• Malignant Tumor Of Colon
• Injury To Liver

Pathways

• Transport
• Fatty Acid Transport
• Cell Death
• Cell Proliferation
• Gene Silencing
• Fatty Acid Oxidation
• Pathogenesis
• Mrna Splicing
• Immune Response

• Cell Growth
• Fatty Acid Beta-oxidation
• Secretion

PTMs

• Oxidation

• Acylation

Research Areas

• Cancer
• Lipid and Metabolism

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/ACSL5

Best Uses of the ACSL5 Marker

This article discusses the ACSL5 marker and its many applications in molecular biology, Clinical research, and cell viability. Although the methods used to capture boster proteins are similar to those that are used for conventional chromatography they still have a place for all scientists. Here are some of its best applications. Continue reading to discover more. Also, you can check out our other bosterbio articles: Best Uses for the ACSL5 Marker

The molecular biology

ACSL5 is a highly expressed protein in the human small intestinal. Non-splicing genotype A contains a small amount of ACSL5 transcription which is known as Spl. We compared the Spl and NSpl forms to discover the effects on function of this variant. We studied the effect of the ACSL5 variant on cell viability and growth.

The ACSL gene family includes more than 60 proteins, and each is a paralogue of ACSL5 gene. In humans the ACSL gene family is comprised of three genes: Acsl1a, ACSL5 and ACSL2b. The ACSL5 gene is conserved across all vertebrate classes, but its paralogue has been removed from other animal species. The study of the ACSL5 gene's molecular biology marker has been a significant step in the understanding of the function of genes and the evolution of human species.

PCR was used to confirm the presence of ACSL5 gene in DNA samples. The ACSL5 marker was utilized in kidney cells of humans (HEK293) and brain cells (MCF-7) as well as in oligodendrocyte cells (HOG). Utilizing a PCR reagent that is supplied by QIAGEN GmbH, we amplified the plasmid's DNA and validated it through Sanger sequencing.

We identified two human orthologues to the Acsl5 and two ACSL3 genes by using the ACSL5 gene. ACSL3 maps to the same area on the human genome, and ACSL4 maps the remaining 2R. The WGD was conducted on this ancestral proto-chromosome and resulted in the splitting of genetic information. Two genes derived from the 2R were later copied independently on the two chromosomes.

Other studies have shown that ACSL5's expression is negatively associated with ER and PR status in breast cancer. ACSL inhibitors, like triacsinC (Abcam) and 2-fluoropalmitic acid (2-FP), also inhibit ACSL activity and cell growth. Thus, ACSL5 may be an effective marker to detect breast cancer. Although it is difficult to predict the precise role of ACSL inhibitors, these results suggest that it may be beneficial in the treatment of breast cancer.

Clinical applications

Nearly all human tumors carry the ACSL5 gene. The ACSL5 gene has been implicated in various human cancers, including hepatocellular carcinoma and renal clear cell carcinoma and seminoma. Utilizing real-time reverse transcription PCR The RNA levels of ACSL5 in LCLs were measured and normalized to UBE2D2 levels of RNA. Primers for ACSL5 were created to amplify the gene by crossing E19-E21 as well as the ACSL5 exon E20.

ACSL4 is part of the acyl-CoA synthetase long-chain protein family. It is implicated in lipid peroxidation-dependent iron death. Its role in generalized cancer is not fully understood. To determine its prognostic ability the marker was examined in a pancancer database. Additionally, gene variation and epigenetic modifications of ACSL4 were assessed using the GSCA and PrognoScan databases.

ACSL3 regulates the biogenesis of lipid droplets and maintenance. It may be implicated in the development of hepatocellular carcinoma and the formation of lipid droplets. ACSL5 is associated with an excellent prognosis for patients suffering from breast cancer with high ACSL3 levels. A new study has suggested that ACSL5 could be a good indicator of prognosis in the beginning stages of breast cancer.

ACSL5 expression was higher in the h284B5F5/M10 cells than in MCF-7 breast cancer cells. These results suggest that the ACSL5 function is regulated in breast cancers with high ER expression. ACSL5 knockdown decreases hepatocyte the synthesis of triglyceride, and ACSL5 overexpression triggers the production of ceramide which is a signaling molecule that plays a role in the apoptosis process. Further research is needed to establish a correlation between ACSL5 expression and lipid metabolites in breast cancer.

ACSL5 expression in MDA-MB-231 and MCF-7 cell lines has been linked with obesity. This is a reliable indicator to determine metabolic conditions. ACSL5 might be targeted in diets and therapies which target obesity. ACSL5 has been shown to be effective in clinical practice, despite its potential complexities. The next step is to apply ACSL5 in clinical research.

In metabolic disorders such as obesity and carcinogenesis, excess metabolic fatty acids are involved. The ACSL5 gene's genetic variant the rs2419621 (the "T allele") has been linked to an increase in fat utilization in tissue cells and cells in the cellular layer. The ACSL5 short protein isoform has also been associated with increased utilization of fatty acids within tissues cells, cells, and various organs. This mutation, which is in the regulatory zone of the ACSL5 promoter is associated with increased fat utilization.

Cell viability

Steven Boster, founder and CEO of Boster Bio, developed the ACSL5 marker that determines viability of cells. Boster Bio was founded in 1993 and has since grown to be one of the biggest Chinese catalog antibody companies. Boster invented PicoKine(tm) which is a unique ELISA platform that utilizes trade secrets to deliver high-sensitivity ELISA kits in the latter part of the 1990s.

Human cells express ACSL5 in large quantities. The gene is highly expressed in the mucosa of the small intestine. While the nonsplicing variant AA doesn't produce much ACSL5 mRNA, it is present in large quantities in the mucosa of the small intestinal. The Spl isoform has a growth inhibitory effect. Spl isoform can be toxic and inefficient translation can reduce its activity.

Many diseases are related to the ACSL5 gene including glioma and sinus adenocarcinoma. It also has important paralogs within the gene ACSL6 and ACSL3. A regulatory region located in the promoter regulates the ACSL5 gene. The metabolic pathway of fatty acids is also affected by fatty acyl-CoA Ligase activity.

Spl RNA detection

Three major transcript forms are encoded by the ACSL5 gene. Two of them are encoded by two AUG-translational initiators. The longer one begins at AUG codon 1 and the shorter one occurs at downstream AUG2. The third is triggered by alternative splicing of the final exon, and is stimulated by the genetic variant rs2256368. Both are expressed in the eukaryotic cells, where the ACSL5 marker can be used to detect SplRNA.

RNA is a key element in cell growth, and the ACSL5 variant is a promising genetic marker for detecting Spl. SplRNA has lower activity than the protein, however it is associated with cancerous cells that have lower levels of ACSL1 or ACSL4. The ACSL5 variant is thought to be involved in the process of lipid metabolism and carcinogenesis.

ACSL5 RNA was expressed in cells in HEK293 at the exact levels as NSplRNA. Additionally, Spl-ACSL5 was deregulated when compared to NSpl forms. The result was a decrease of Spl-protein levels, which suggested that the protein was translated inefficiently. This indicates that Spl RNA is harmful when incorporated into DNA.

The ACSL5 antibody was successful in detecting SplRNA in LCLs. It displayed a high correlation coefficient with similar band profiles to other isoforms, which indicated that the rise in SplRNA was correlated with the reduction in ACSL5 protein. In fact, the reduction in ACSL5 protein corresponded to significant increases in Spl RNA levels in LCLs.